When it comes to having a sweet tooth, bacteria take the cake. Which is why, in a new study in mice and lab-dish cells, researchers were able to use the sweet stuff to lure bacteria out of hiding and kill them with antibiotics.

The bacteria the researchers targeted were so-called “persisters,” a subpopulation of bacteria that evade antibiotic drugs by playing dead — they hide out in a dormant state and then flare up again later, after the threat of drugs has passed. (This mechanism of drug-avoidance is different from the one used by antibiotic-resistant bugs like MRSA, which acquire genetic mutations that protect them from the drugs.)

The goal of the new study, was essentially to use the sugar to wake sleeping bacteria, to “get them up off the ground so we can punch them and knock them out,” senior author James Collins, a professor of biomedical engineering at Boston University, told the Boston Globe.

The researchers looked at two common and often persistent bacteria: E. coli, which can cause urinary tract and gastrointestinal infections, and Staphylococcus aureus, which cause staph infections. Both bugs are susceptible to the antibiotic gentamicin, one of a class of antibiotics called aminoglycosides.

The researchers combined gentamicin with different kinds of sugars, including mannitol, fructose and glucose. (Sucrose, the stuff you put in your coffee, is just one of many types of sugars as far as biochemistry’s concerned.) When the scientists added these sweetened antibiotics to bacteria grown in Petri dishes, it killed over 99% of the bacterial persisters. The type of sugar seemed to make a difference, as well; only fructose helped the drug kill S. aureus, for instance.

The researchers were also able to add sugar to antibiotics to treat urinary tract infections in mice.

If the same technique worked in humans, it could aid in the treatment of chronic, recurrent infections like strep throat, staph and urinary tract infections, and tuberculosis, which are typically caused by bacterial persisters. Doctors could simply enhance the effectiveness of existing antibiotics, instead of waiting for new ones to be discovered.

Of course, the trick would be getting the sugar to the infection site; humans would likely digest it before that could happen. (The mice in the study received the sugar and drug intravenously.) But mannitol, one of the sugars used in the study, isn’t digestible by people.